----start medsurg.lec.03.19.98-----

medsurg
3/19/98
brockman

brachycephalic airway obstruction syndrome

we have the unfortunate honor 
of having 4 hours of lecture with Dr. Brockman at this time (he said 
that). we'll start with surgical conditions of the airways, and then 
we'll move into surgical conditions of the ear. to add insult to injury, 
we have to deal with his aussie accent. 

for exam purposes, everything 
you need to know is in the handout. we'll go over some stuff not in the 
notes during lecture, but that's just for completeness, so do not panic, 
everything you need to know is in the handout.

so, the actual title of 
the lecture today is "brachycephalic airway obstruction syndrome" but 
that's just what we're starting out with.

slides: a bulldog and a 
squishy face cat.

we've done a hell of a job with selective breeding - 
we'll never be short of work with airway disease given the popularity of 
brachycephalic breeds. this syndrome is a direct result of this selective 
breeding which has resulting in the flat faced conformation in cats and 
dogs. a foreshortened calvarium, without soft tissue changes in 
accordance with the skeletal changes. so there is too much soft tissue to 
go along with the skeletal size. these changes can cause life threatening 
debilitations. 

feline patients do have the same syndrome but are rarely 
clinically affected with classic brachycephalic airway obstruction.


brachycephalic airway obstruction syndrome is comprised of dyspnea 
associated with four things:

1. stenotic nares
2. elongated soft palate 
(failure to shorten, really)

these are the two primary conditions. 
secondary to those defects and secondary to chronic subatmospheric airway 
pressure we see

3. eversion of the laryngeal ventricles
4. laryngeal 
collapse, permanent abduction of laryngeal structures

when we look at 
the larynx and pharyngeal area on rads, we would normally expect a thin 
soft palate just contacting the epiglottic cartilage of the larynx 
occupying the common pharynx. clinically affected animals with this 
syndrome frequently have a very broad soft palate extending well beyond 
the epiglottic cartilage.

animals with obstructive disease, and almost 
every brachycephalic dog has some degree of airway compromise - the 
owners get used to the snuffling sounds when it breathes in and out - 
need to be assessed to see if the compromise is causing clinical disease 
or not. typically, owners of affected dogs will complain of excercise 
intolerance in the dog. some owners report episodic collapse, some astute 
owners will describe color changes in the mucous membranes during 
collapse. frequently they describe a change in the noise the dog makes - 
more intense, more vibrant. in extreme situations, animals with this 
problem, especially during stress, hot days, excercise - can suffer 
periods of acute respiratory obstruction and prevent in acute respiratory 
arrest and cyanosis - although most animals don't do that, it is 
reported. 
the emergency group will talk about management of animals with 
acute respiratory obstruction - we won't talk about it now, suffice it to 
say that you should always be equipped to deal with acute respiratory 
obstruction and to secure an airway by some means. since tracheotomy tube 
placement may be needed, we'll go over a technique for that later.

for 
the most part these dogs present because of the owner seeing exercise 
intolerance or hearing loud respiratory sounds and occasional collapse. 

we have to see if there are other underlying reasons for this. we have to 
interrogate carefully the respiratory tract (lower) and cardiovascular 
system, two other areas where problems could cause these signs. 
musculoskeletal disorders could do it too, so you have to do an ortho 
exam. logically, your investigation will include cbc/chem/chest rads. 
also you shouldn't think that if an animal hasn't had a problem before, 
it isn't going to get one. other non-disease situations can exacerbate 
the respiratory compromise, like obesity, endocrine disorders which may 
result in redistribution of body wt, like hypothyroidism, cushings, etc. 
so, just because there was no problem before doesn't mean it will be ok 
today.

these conditions can be treated. we want to determine that the 
airway compromise is the problem before we treat it, though. nostril 
narrowing can be simply treated by resection of a small wedge of tissue 
from external nares. soft palate can be easily trimmed through the oral 
cavity simply by placing artery forceps or hemostats across it, using 
tonsillary crypts as a landmark, and oversewing the end. finally, everted 
laryngeal saccules can be resected by grabbing them and cutting them out 
at their base.

the nostril narrowing following LaPlace's law of flow is 
probably most influential in restricting airflow through upper airways 
when the animal is nose breathing. (if mouth breathing, soft palate is 
more influential). 

looking at the soft palate, you can see the 
compromise this can cause - on the left, we are looking at the larynx 
from the nasopharynx - we see the dorsal palatal mucosa and the esophagus 
which is dorsal to the larynx, and the dorsal rim formed by the arytenoid 
cartilage, and the soft palate, the caudal tip of which is nearly totally 
obstructing our veiw of the larynx. the tonsilar crypts are ventral to 
this tissue - we can't see it in this view. 
on the right, post 
resection, we see the normal view of the soft palate, just overlapping 
the epiglottic cartilage, allowing us to see the whole remainder of the 
epiglottic cartilage, the processes of the arytenoids, and the opening of 
the larynx. this is much more normal.

again - the epiglottic cartilage 
hangs down in front, thorugh which you see the vocal folds. the lateral 
ventricles are between the vocal folds and the epiglottic cartilage's 
caudal border. we see the corniculate process of the arytenoid protruding 
as well as the cuneiform process. the area between the vocal folds and 
the caudal epiglottic cartilage should be free from any tissue.

slides: 
a real case  - 2 yr old bulldog. looking directly through the open mouth 
at the rostral tip of the epiglottic cartilage. we see the tonsillar 
crypts clearly in young dogs on either side. as we're looking at this 
dog, we want to decide how much soft palate to resect. be conservative - 
you can always take more off, but you can't put more on. if you take off 
too much, you lose soft palate function, which is not only to divide oro 
and nasopharynx, but to occlude nasopharynx during eating and stuff, and 
you end up with food in the nose, chronic nasal d/c, and so forth. in 
non-bulldog breeds, you trim the soft palate to the level of the caudal 
tonsillar crypts. in bulldogs, you can go about halfway up the tonsillar 
crypts. if you aren't sure, stay at the caudal aspect of the crypt. do 
this by gently grasping the caudal soft palate with tissue forceps and 
pull forward. place hemostats across at the level of the caudal tonsilar 
crypts. cut with scissors, and oversew the stump you've left with fine 
monofilament absorbable suture for hemostasis. that's it. pretty easy. 
now, most of you have noticed there was no ET tube in these slides. 
that's because we generally do this with a tracheostomy tube in place. 
the lateral ventricles of the larynx, when everted - you see two balloons 
obstructing your view of the vocal folds. you use allis tissue forceps to 
gently grasp the everted ventricle, and with long handled scissors you 
excise the ventricle at its base, trying NOT to damage the vocal folds or 
other tissue hanging out at the ventral aspect of the larynx. if you 
damage things, scar tissue will form and you get ventral laryngeal 
webbing - exuberant scar tissue forming further obstruction. so be very 
careful. remove only the ventricle, do not lacerate vocal folds.

finally 
on the way out, you do the nostrils - this is a shar pei here - the 
untreated nostril is very narrow. the nostril with tissue removed from 
the alar fold has a much larger opening. procedure is in the notes. the 
tissue removed is a small triangle oftissue - 5-7 mm.

the most worrying 
consequence of brachycephalic airway obstruction syndrome
is complete 
laryngeal collapse. very hard to treat. happens generally only in very 
young animals with complete obstruction. due to subatmospheric pressure 
in airway structures are totally sucked in. laryngoplasty sutures 
frequently fail, so you would ideally treat prior to this event.
key 
points: nearly all brachycephalics have some obstrucxtion. carefully 
evaluate for other diseases which may be exacerbating it or totally 
accounting for the present clinical signs (like pulmonic stenosis in 
bulldogs). you want to use a tracheotomy tube during anesthesia. longterm 
prognosis is good if you treat at young ages, and worse if you treat when 
they are older. owners of these animals should be counseled to keep pets 
at normal weight.

word of caution: Dr B has yet to have had to resect 
the soft palate of a non brachycephalic breed, so be cautious - if you 
think a dog has airway obstruction, don't jump to resect the soft palate 
of a non brachycephalic breed. remember, a 2D view of the soft palate on 
rads isn't helpful. look at it yourself in the dog. rotation of skull can 
make rads misleading.

tracheal collapse or tracheal disease per se is 
not part of brachycephalic airway obstruction syndrome, although it may 
be concurrently present.

a final note: these dogs never had it so good 
when you anesthetize it. it's much easier for them to breathe with the 
tube in, so generally the dog enjoys it :) normally, you remove the ET 
tube when animal starts waking, but these dogs need ET tube left in as 
long as possible. try to do these dogs at the beginning of the day - this 
helps you to keep a close eye on them during the first 4-6 hrs 
postoperatively. 

moving further back into the airway: primary laryngeal 
conditions:

the larynx in a neutral position is compared to the larynx 
of a brachycephalic with laryngeal collapse - the arytenoids are totally 
apposed, no room for air to pass b/w them. this is very hard to treat.


laryngeal conditions we see:

1. lateral ventricular eversion
2. 
laryngeal collapse
3. laryngeal paralysis (congenital in bouvier, husky; 
also acquired secondary to neck trauma, neoplasia, other - idiopathic - 
polyneuropathy? endocrinopathy? dalmations may have congenital 
polyneuropathy with laryngeal dysfunction; also myasthenia gravis may 
cause)
4. chondroma/chondrosarcoma of larynx; rhabdomyosarcoma. in cats, 
LSA, SCC.

if you suspect laryngeal paralysis, do cbc/chem/rads as 
minimal database.

anatomy: larynx is made of different cartilages - the 
cricoid, that attaches it to the trachea; the thyroid, which forms 
lateral limits of the larynx, the arytenoid, which is the mobile part 
articulating rostrally with the cricoid and which fine tunes the diameter 
of the airway; and rostrally the epiglottis. all of this is suspended by 
the hyoid apparatus. the esophagus is dorsal  and soft tissues of the 
neck are ventral to the larynx. 

functions of the larynx are: 
creation 
of noise 
fine tuning of airway diameter to meet current needs.

when 
larynx loses function, things happen:
1. loss of ability to close during 
swallowing - loss of airway protection - often manifests as chronic cough 
due to aspiration
2. fixed upper airway obstruction - can't respond to 
increasing needs for air, resulting in exercise intolerance
3. reduced 
alveolar ventilation
4. loss of vocalis muscle control - can't bark, 
meow, or pitch changes

clinical features of laryngeal paralysis:


exercise intolerance
chronic cough
stridor/increased inspiratory noise 
"l'homme qui skie du bois" (man sawing wood)
cyanosis/collapse
dysphonia

aspiration pneumonia

the acquired form of idiopathic laryngeal paralysis 
is seen in labs, afghans, st. bernards often. 

diagnosis:

1. signalment 
(breed predilection, age predilection for old/middle aged animal)
2. PE - 
usually normal at rest, abnormal with excitement - cyanosis, stridor
3. 
rule out congenital and other acquired forms:
-neoplastic
-polymyopathy

-polyneuropathy
-endocrine
4. TBFVL - tidal breathing flow volume limits 
- not practical, involves using a face mask and taking airway resistance 
measurements and gasp volume measurements. affected dogs have abnormal 
peak flow - flat line
5. direct observation of laryngeal movements under 
light plane of anesthesia - this is our gold standard at the moment and 
it isn't very sensitive.

slide: lab with laryngeal paralysis. it's also 
hypothyroid and has coxofemoral disease. no intrathoracic pathology. no 
neck pathology. has stridor and cyanosis and open mouth breathing during 
stress. looking at this dog's larynx, we see an absence of movement in 
the arytenoids - it's fixed in one position. 

we hope that during a 
light plane of anesthesia, you can watch the airway open during 
inspiration. if it doesn't, you assume there is paralysis. however, 
sometimes, animal larynx is in neutral position, and there is apparent 
movement of the arytenoids during inspiration due to low pressures, and 
then they bounce back - but there isn't really abduction during 
inspiration. you want to correlate ventilation with laryngeal movement. 


if the larynx appears closed and never changes, you have laryngeal 
paralysis.

Treatment: 

Unilateral arytenoid lateralization - tieback 
procedure (also used in horse)
the paralysis is bilateral, but when doing 
an extralaryngeal approach in dog, we just do one side - that's enough to 
make the dog comfortable. 

1. extralaryngeal approach
2. unilateral 
procedure - best for speed, reduced risk of postop complications like 
aspiration
3. disarticulate the arytenoid from the thyroid and cricoid 
cartilage and cut communication b/w left and right arytenoid
4. sutures 
secure arytenoid in abducted position. from cricoid cartilage to muscular 
process of arytenoid or from caudal thyroid to muscular process of 
arytenoid, so arytenoid is pulled caudally or caudally and laterally.


most right handed surgeons do this with dog in RLR so they do left side. 

incision is just ventral to lingual-facial branch of jugular coming off 
from internal maxillary.

approach is straightforward. you just go 
through subcu fat (although there may be a lot of that...) once you 
dissect to the larynx, you can feel the cartilage. first you meet the 
thyroid cartilage, and you cut the thyropharyngeus muscle, reflect the 
cartilage laterally, and visualize the cricoid and arytenoid cartilages. 
now place a suture from caudal cricoid or caudal thyroid around the 
arytenoid muscular process, and pull.this will pull arytenoid caudally 
and laterally, out of the airway. 

slide: postop view - instead of a 
slit, the airway is now a triangle - adequate for comfort of dog. do it 
in the morning, give steroids and observe in postop period. 


complications include airway edema and hemorrhage, so you need close 
observation.

-----break----

ok. we just about finished talking about 
extralaryngeal surgical repair for dogs with acquired laryngeal 
paralysis. we don't really know the real cause of this disease - it's 
neurogenic atrophy of the laryngeal musculature, and degeneration of 
recurrent laryngeal nerve. you can do arytenoid lateralization on dogs 
with known cause of paralysis also - dogs with traumatic disruption of 
the recurrent laryngeal n., or as a palliative procedure if there is 
neoplasia involved. prognosis in those cases is different, revolves more 
around prognosis of underlying dz.

short term complications of the tie 
back are edema and hemorrhage

intermediate complications: 

1. 
aspiration - that's why we do unilateral procedure - if bilateral, risk 
of aspiration would be much higher. most dogs you do this to will cough 
more at first, esp after drinking, but will compensate w/in a few weeks.


there are many techniques for treatment - the one we just heard about is 
Dr. B's favorite, he thinks it has least risk for longterm complications. 
other people have other preferences. 

Intralaryngeal techniques:


involve resection of the vocal folds, or resection of part of the 
arytenoids and the vocal folds, unilaterally or bilaterally. 

a vocal 
fold resection is done through the oral cavity - you insert scissors into 
the ventricle and make a cut in the ventral vocal fold and another cut - 
opening the airway. you could also do this through a ventral laryngotomy 
incision. then you'd cut the ventral cricoid cartilage to get access to 
the folds. 

Dr. Brockman doesn't see the point of risking complications 
of ventral laryngeal scar formation when the other technique works well. 
you have to perform tracheotomy if you do vocal fold resection, because 
hemorrhage and edema will compromise the airway for at least a couple of 
days postop. Dr. Holt might disagree with this.

People have described 
intraoral approaches using sharp biopsy forceps to nibble at the 
arytenoids. Dr. B considers this a salvage procedure - why enter the 
laryngeal lumen when you can do a good extralaryngeal procedure.

If all 
else fails, you can do a permanent tracheostomy.

slide: tracheostomy, 
ventral view

this is a difficult surgery, should be done by a 
specialist. patients with permanent tracheostomies should end up with a 
good patent airway. swimming is permanently contraindicated 
postoperatively, as is running through very long grasses. this is a 
salvage procedure for end stage neoplastic or paralytic airway disease.


summary: laryngeal paralysis can be congenital (husky, bouvier) or 
aquired (secondary to neoplasia, polyneuropathy, polymyopathy) (or 
idiopathic in labs, afghans, st. bernards) and are best treated with the 
unilateral extralaryngeal procedure called the tieback.

Laryngeal 
Neoplasia:
laryngeal neoplasia is rare. most common in canines is a 
rhabdomyosarcoma or oncocytoma (same thing, different nomenclature). in 
cats most common is SCC, or LSA. 

main presenting signs:

1. exercise 
intolerance
2. stridor
3. change in bark/meo
(all signs of fixed airway 
obstruction)

slides: 10 yr old cat with presenting complaint of 3 wk 
history of "loss of meow" and progressing dyspnea.

lateral rads show air 
filled trachea in the neck with abrupt narrowing in laryngeal region - 
the lumen size should be constant through the larynx, but here it is not. 
grossly, you can see a large LSA mass sitting on the epiglottis. now, you 
could treat LSA medically, but this degree of airway compromise was so 
severe that they euthanized the cat. otherwise would have needed to put 
in trach tube, debulk tumor, follow with chemo.

how clever cats are at 
disguising disease until they are very very ill is something that will 
probably continually surprise you. if you had anesthetised this animal 
and tried to put in an ET tube, you'd have  been really screwed (my 
wording). you have to be prepared to put in a trach tube. sometimes, just 
the  PE can stress the cat so much that there is an acute respiratory 
crisis. same with thoracic disease - severe pleural effusions may be 
hidden by the cat until they are near crisis state, and stress of PE 
causes decompensation. be really careful with dyspneic cats!

canine 
patients on the other hand tend to get skeletal mucle tumors - 
rhabdomyosarcomas - and we think they may be congenital b/c they happen 
in really young dogs. congenital rhabdomyosarcoma also occurs in dog 
bladder. anyway the dogs present with dyspnea, changed bark, progressive 
dz. tx for rhabdomyosarcoma short term is debulking surgery, with trach 
tube in place,  and long term tx with radiation therapy. 

if long term 
therapy isn't an option, complete laryngectomy is an option. it's very 
difficult, though - use a surgeon. put in a trach tube and ship the dog 
to a specialist.

fortunately, laryngeal neoplasia is very rare.

Surgery 
of the Trachea:

avg dog/cat has 35-40 incomplete hyaline cartilage 
tracheal rings joined at the top by a dorsal tracheal membrane of CT and 
respiratory epi. blood supply is segmental, from thyroid and 
tracheobronchial arteries. fortunately, surgical dz of trachea is rare.


collapsing trachea: affects toy/mini dogs. tracheal collapse comes about 
because these tiny dogs lack sufficient proteoglycan in the cartilagenous 
rings, making them less able to withstand subatmospheric pressure i the 
airway, making them predisposed to collapse. probably all tiny dogs, esp 
yorkies, poms, have a predisposition to this, though not all will develop 
it. often, it takes another factor in combination with the predisposition 
to cause th problem. these can present as middle aged dogs post 
respiratory infection, or with concurrent endocrinopathy or cardiac 
disease. it then becomes a juggling act of threating the concurrent 
problems and prioritizing which need medical and which need surgical 
intervention.

the only clear cut sx candidates for surgical tx of 
tracheal collapse are young dogs, 6 mos - 4 yrs, whose primary condition 
is airway collapse due to soft tracheal cartilage. surgery may help some 
older dogs with concurrent disease, but it is hard to select which ones 
it may help, and those dogs are poor surgical candidates due to other 
diseases.

clinically these dogs present due to:

1. exercise intolerance

2. honking sound, worse with stress, heat, excitement
3. pretty normal at 
rest

we investigate these animals and exclude other conditions, so we do 
cbc/chem/chest and neck rads. we're looking for evidence of narrowing of 
the trachea on the rads. this may be most obvious at the thoracic inlet. 
take inspiratory and expiratory rads to see if the diameter changes. 
also, don't overinterpret your rads - the esophagus may drape over the 
trachea, giving the impression of tracheal collapse. look really 
carefully. 

not all dogs will show tracheal collapse on plain film rads. 
if you rule out other diseases and don't see it, you can try fluoroscopy 
- put the animal under the tube and induce a cough and see if the airway 
collapses. this is a useful way to look at these animals. you can see 
tracheal and mainstem bronchial collapse. another technique is 
bronchoscopy  - you can directly visualize a collapse. takes skill.

this 
occurs in varying degrees.
slides: cross sections through normal trachea 
- the dorsal ligament is flat and the ring is round so it makes a D. 
there is a gradation from cranial to caudal.
slides: cross sections 
through affected trachea - trachea contains variable amounts of foam. the 
dorsal longitudinal ligament is very long in some areas, with flat 
cartilage instead of C shape. there is no real lumen.

you can make this 
dx well on PE - feel the neck. on fat animals this isn't that helpful but 
otherwise, see if you can occlude the airway with light digital pressure. 


also, consider the treatment options - medically, you can manage these 
animals pretty successfully with antiinflammatories and antitussives and 
tx underlying dz - eg, if heart dz, treat that and give steroids and 
antitussives like butorphanol to reduce coughing. coughing and 
inflammation is a vicious cycle, and if you break it that can really 
help. if animal is overweight, put it on a diet. when you consider the 
appearance of these slides, though, if htere is no concurrent disease, 
you want to enlarge the lumen. how? take a nylon prosthesis, suture it 
around the trachea, and then suture the longitudinal  ligament to the 
prosthesis.

slide: rads from a 3 yr old dog with no other disease except 
tracheal collapse

the prosthesis is aabout 1.5 cm in diameter, is round, 
made of syringe casing. has a few holes in it. you use four or five of 
the single rings in different points along the airway, to minimally 
interfere with blood supply. you slide them around the trachea, and 
suture them to the tracheal rings, and dorsally suture the membrane to 
them. this is touchy - you have to avoid the recurrent laryngeal nerve, 
and in tiny nerves, that nerve is like a thread of cotton next to the 
trachea. laryngeal malfunction is often concurrent with tracheal 
malfunction in these dogs, so evaluate it preop and postop. laryngeal 
paralysis might need to be fixed at the same time as the tracheal 
stenting procedure. 
also avoid the vessels of the neck, esophagus, etc. 
this is something you don't want to do right out of school - send it to 
specialist.

so, tracheal collapse summary: happens in many toy/mini 
breeds, best prognosis in dogs with no other condition, tx w/tracheal 
prostheses (external to trachea).

Tracheal Stenosis: tracheal stenosis 
is not the same as collapse. this is seen in brachycephalics, but isn't 
part of classic syndrome. it's  an unusual condition that seems to occur 
not due to weak tracheal cartilage, but by cartilage that fails to 
unfold, and stays overlapping at the dorsal aspect. although tracheal 
stenosis is common in brachycephalics esp bulldogs, boston terriers and 
french bulldogs, we're not sure how much it really causes a problem. we 
often see this on radiographs. when the trachea is stenotic like this it 
can be very hard to put in an ET tube - that's the key problem.

next 
most common indication for surgery on the conducting airway is airway 
rupture. the most frequent time we see this is following trauma to the 
neck. dogfight, BDLD interaction, etc.

airway rupture, clinical signs:


1. free air around trachea creating emphysema in head, neck, or 
mediastinum
2. pneumothorax secondary to above
3. hemoptysis (maybe)
4. 
dyspnea - usually, to varying degree although less than expected.

slide: 
ventral neck - a few puncture wounds, bruising, very swollen neck. this 
is a little dog. you can't ignore this just b/c it looks like skin 
wounds.

tracheal damage may also occur secondary to overinflation of ET 
tube cuff. Be careful with these, esp in cats which may be more prone to 
this problem. 

slides: rads from that little dog with bite wounds.

we 
see a lot of subcutaneous air next to the thoracic wall, and above the 
dorsal thorax and in the neck. this dog has severe subcutaneous emphysema 
secondary to the trauma. this may be due to air getting through bite 
wounds, or through disruption of airway - with this severity suspect 
airway trauma.  we also see very clear view of brachicephalic trunk, 
subclavian artery, etc in mediastinum- so there is probably a 
pneumomediastinum. we also see a great view of the right atrial appendage 
because there is a pneumopericardium. 

slides: surgical approach to this 
dog. we see some very grey muscle and devitalized tracheal cartilage, and 
we see the ET Tube also. there is also a large abcess around the trachea. 


slides: cat - 6 mo old female cat was spayed and 2 days later blew up 
like a balloon. the owners picked it up and felt the crunching and 
brought it in. it wasn't dyspneic, but was inflating. endoscopy showed a 
red area in trachea. a ventral midline approach to the trachea revealed a 
defect in the trachea adjacent to where the cuff of the ET tube would 
have been at the prior surgery. this was repaired with simple interrupted 
sutures suturing the ligament back to the cartilage.

slide: a similar 
case in a dog that had had surgery 6mos prior. presenting complaint was 
paroxysmal coughing q 4-5 days. dog would inflate during coughing, owners 
would massage air down to hind end and it would go away, then it would 
happen again later.  a hole was found in trachea, as above. they resected 
a portion of the trachea, placed a tracheostomy tube in the healthy site, 
lifted out the bad part, and reanastomosed the ends. this is a yorkie, 
and there isn't much to play with -usually you want to suture cartilage 
to cartilage to ensure fibrocartilage healing, otherwise you get fibrous 
CT and potential for later stenosis. most dogs you can take out 3-10 
rings w/o too much concern. postop, dog didn't inflate any more.


intrathoracic tracheal avulsion in cats - presumed post traumatic. 
present with progressive dyspnea and funny bubble thing on chest rads - 
the mediastinal membrane walls off the injury and you see this on the 
rads - it takes time for fibrosis to create stenosis, which is why it's 
progressive. surgically you open the membrane, resect and anastomose the 
trachea intrathoracically.

slide: traumatic tracheal disruption in dog 
post fight. crushed cricoid cartilage, tracheal laceration - had to 
anastomose cartilage to cartilage and resect the cricoid.

tracheal 
neoplasia: very very very rare. Dr. B. hasn't ever seen it. 
slides: 
radiograph of cranial chest - we see just caudal to the scapulohumeral 
joint a little soft tissue density in the lumen of the trachea. this part 
of the trachea was resected - it turned out to be a deciduous tooth that 
got inhaled, embedded

don't forget about filaroides osleri - you see 
nodules in the trachea and bronchi. have to screen fresh feces for 
larvae, or sometimes you find them in sputum. 

finally, how to put in a 
temporary tracheotomy tube:

have a selection of tracheotomy tubes. dogs 
with large tracheas should have the silastic tubes with a low pressure 
high volume cuff. smaller animals should have the silver plated metal 
tubes with an inner canula that you can remove and replace for cleaning 
(frequently).

to place the tube, hopefully under aseptic conditions, 
assuming this is elective, you put the dog in dorsal recumbency and prep 
and drape the ventral neck. make a midline incision. get through fat. 
you'll be right over the sternothyroideus and sternohyoideus. separate 
those muscle bellies through the natural cleavage line. then you see the 
tracheal rings. place a stay suture all the way aroudn the rings proximal 
and distal to your proposed incision site. then, make a transverse 
incision in the trachea, about 1/3 to 1/2 way across the trachea. you 
will see the ET tube in there. don't CUT the ET tube. now select a 
tracheostomy tube to occupy about 2/3 the diameter of the trachea. have 
the ET tubbe removed and insert the trach tube. hook your machine to the 
tube so your dog doesn't wake  up. put in some skin sutures around the 
tube. secure thewhole thing with special tape.

slides: trach tube 
removed from dog showing plug of secretions occluding the lumen. a dog 
with a trach tube in place can't be left alone - you have to stay with it 
and make sure the airway doesn't become occluded. most big dogs don't 
have a problem with secretions over the first 24/48 hrs, but you have to 
clean it every 4-6 hrs. small dogs are a really big problem, because they 
can fill up really quickly, as can cats.

---break---

someone asked 
about debarking - that's a vocal fold resection. it's not done for 
medical reasons, so he's not talking about it here. CO2 lasers have been 
used for this. Debarking is illegal where Dr. Brockman is from so he 
doesn't want to talk about it.

The next two hours are devoted to 
surgical conditions of the ear.

otitis externa and otitis media comprise 
the bulk of what we'll discuss.

note that the otoscope cone has been in 
use for a really long time as per this slide he's showing us from a 
really old book. you need long cone - not human type.

anatomy:


cartilages: scapha (Pinna), tragus, scutiform, annular - see handout. 

inner ear has vertical canal and horizontal canals supported by the 
cartilages.  the tragus is really part of the scaphy, the proximal part.  
the pretympanic bone is close to the facial nerve which is between it and 
the parotid and mandibular salivary glands. 

the middle ear cavity is a 
cuplike thing in the petrous temporal bone and has poor drainage. the 
main drainage is via eustachian tube; other communication besides eardrum 
is with ossicles and oval window and round window. 

look at drawings in 
handout!
cats have a big section of sympathetic nerve within the middle 
ear. dogs have that in a bony canal next to the middle ear.

some simple 
conditions of the pinna:

Ear Hematoma: anyone who's worked in a practice 
will have seen this. Aural hematoma occurs secondary to rupture of the 
great auricular artery. the rupture is caused perhaps by trauma (blow to 
the ear, chronic head shaking due to infection), or is perhaps immune 
mediated and related to vasculites. Dr B thinks most of the cases are 
trauma related. in people, this would be cauliflower ear, as in rugby 
players, or boxers. 

slide: aural hemotoma - big puffy pinna - looks 
like a pierogie. to diagnose this, stick in a needle, aspirate some fluid 
- will see serosanguinous fluid.

these are probably traumatic - are 
tightly related to uncontrolled otitis externa. you have to treat the 
underlying disease or the thing will just recur.

treatment for hematoma: 
there are many. Dr B prefers to incise the medial aspect of the pinna and 
drain the fluid, then loosely place a series of vertical mattress 
sutures, placed in an orientation that doesn't interfere with blood 
supply. leave them a couple of weeks. hopefully you get fibrous unions 
b/w the cartilage and the overlying skin to prevent recurrence. 
classically, people make an s shaped incision on the medial aspect of the 
pinna.

other tx: place penrose drain, leave in 2-3 wks. seems to work. 

key thing is to ID underlying conditions and treat them well.
some people 
use bovine teat cannulas in the ear for a drain - they work pretty well, 
but occasionally they get sucked into the ear.

trauma to the pinna - 
owner always sees this as an emergency, because of great blood supply it 
bleeds a lot. dogs do not generally bleed to death from them but they are 
messy.

three types - superficial laceration through one layer of skin

laceration through one layer of skin and cartilage
full thickness


carefully evaluate wound, remove devitalized tissue, debride edges, close 
wound. for partial thickness, just skin closure - for full thickness, two 
closures. 

hemorrhage will persist around your sutures. you can bandage 
a pinna, but you must be very careful not to put too much pressure on the 
laryngeal area. 

slide: unusual situation - boston terrier got his ears 
chewed by littermates.  looks like got cut w/pinking shears. they trimmed 
the edge surgically and put in some sutures (full thickness closure)

we 
won't hear about ear cropping - it's illegal where Dr.  B comes from so 
that's that. he doesn't care to discuss it.

slide: SCC on pinna of white 
cat. ulcerated mass, full thickness erosion of pinna. these cats get 
multiple sites of tumor frequently. you must carefully check the other 
ear and around the eyelids. tx for these cats is pinnectomy with wide 
margins. for eyelids, there are new photodynamic therapies - you give a 
special drug which localizes in tumor, then expose to UV light - the drug 
when exposed to UV light ablates the tumor cells at that site.

slide: 
dog with similar tumor on pinna - another SCC. note that this smelled 
really bad.

so, that's the story with the pinna.

Now, about Otitis 
Externa:

the flow diagrams in the handout belong to someone at the U of 
Bristol.they outline a logical way to consider otitis externa. we tend to 
think of it in terms of trigger factors and perpetuating factors. put 
simply, it's inflammation of the external ear canal. very very common. 
diagnosis isn't the hard part. dogs that come in shaking their heads and 
with inflamed ears are commonly seen.

trigger factors:

1. mites 
(otodectes cyanotis)
2. foreign body (rare except in CA where there are 
foxtails all over)
3. dermatitis *very* important. any derm problem can 
manifest in ears - skin here is very sensitive. often derm problem may 
show up in ear when it isn't visible anywhere else, so you have to 
consider atopy, food allergy, etc.
4. pyrexia - ear skin can be inflamed 
just due to fever - ear skin is very sensitive to changes
5. neoplasia
6. 
otitis media -could be primary event, resulting in otitis externa - esp 
in cats, with inflammatory middle ear dz
7. microbial infection - 
pseudomonas, proteus spp

why do we divide into perpetuating and trigger 
factors? once inflammation is set up it is self perpetuating.

final 
common pathway seems to be that with any of the above trigger factors, 
you get a change in the microenvironment of ear canal. you get 
inflammation or something that reduces circulating air in horizontal 
canal, changes humidity in canal, changes temperature in canal, favoring 
bacterial proliferation. sometimes also yeasts. once they get 
established, they incite further inflammation which further reduces 
circulation. this concept is key in thinking about surgical procedures we 
might use to break this cycle. 

perpetuating factors:

1. ascending 
otitis media (that we failed to diagnose, so that external ear gets 
reinfected all the time)
2. poor ventilation (because we poorly 
controlled the inflammation, or due to conformation, or other factor such 
as excess wax or whatever)

causes of poor ventilation:

1. inflammation

2. integument hyperplasia
3. poor aural conformation
4. wax buildup


hopefully most of them are caused by some inflammation which we can 
reverse by identifying the trigger and removing it. once inflammation 
becomes irreversible, as in hyperplastic ear disease, we need non-medical 
therapy to remove that extra tissue. if the animal has poor ear 
conformation, you're screwed from the outset. cocker spaniels leap to 
mind. also, some aniamls just build up lots of wax which gets caught in 
hair - think poodle.

slide: otodectes, your little friend :)

the ear is 
full of classic black waxy d/c, common in cats with ear mites, also seen 
in dogs. young pups and kits with this type of d/c probably have mites. 
just take a qtip, smear it on a slide, and look under a microscope and 
you'll see the mites. the important thing about treatment is to use an 
acaricidal prep - don't try to drown them in antibiotics ! also, treat 
your carrier pets. if the dog has it, and there are two cats in the 
house, you have to treat the cats also.

other triggers - the foxtail 
from california, the grass seed of the wild oat that grows there. these 
animals present acutely following a run in the field. they are 
headshaking, pawing ear, etc. rapid onset strongly suggests this type of 
problem. also, tumors - you have to do otoscopic exam to find tumors that 
are halfway down the canal. if you've been treating an animal for 6 mos, 
you must attempt to find the trigger!!

(hopefully you look for it 
earlier than that!!)

some changes seen in the pinna which suggest 
chronicity of the disease:

mild inflammation, wax buildup, irregular 
appearance to integuement - early chronic change. earlier it would be 
smooth epithelium with erythema. early hyperplastic change causes a rough 
appearance.

plucking hair from dog ears can be a trigger that incites 
otitis externa. if the dog already has otitis externa you may need to 
pluck hair to improve ventilation. but if there is no disease, don't 
pluck!!

more chronic than before - varicose changes, hyperplasia of the 
yadayada notches of the pinna, more rough surface

worse still - severe 
proliferative inflammatory change aroudn the external meatus

most 
horrible- looks like brain coming out the ear. teeny tiny opening to 
external meatus with pus dripping out, and what looks like a lot of 
cruciferous tissue growing all over the pinna.

palpate your dog's ear 
canals to feel the elastic nature of their ear canals. the dog in the 
horrible picture has a rock hard ear canal - it gets mineralized with 
chronic inflammation. 

other - 
severely ulcerated skin due to a really 
unpleasant pseudomonas infection

don't think all otitis externa is 
surgically managed. most are managed medically. it's important to id the 
initiating cause and any perpetuating factors, though! we talked about 
external appearance and PE of ear. not every client with a dog with 
otitis externa will let you sedate the animal and do a good exam on their 
first visit (for 90 bucks). but in theory, every aniaml with otitis 
externa should have that kind of workup. some dogs will let you do an 
otoscopic exam without sedation, but those are the exception. so, you're 
being forced to compromise.

dog comes in - shaking head for 3 days. 
right ear red. dog won't let you palpate. acute otitis externa. you're 
not in california - probably not foreign body. what can you do? try 
treating with a polypharmaceutical prep that MUST contain some 
antiinflammatory -dispense something - most have abx, antiinflammatory, 
analgesic, and cerumenolytic. show them how to treat, tell them to do it 
2-3 x daily. tell them, though, that you have to see them again within a 
week, and that if things aren't better by then, you will need to pursue 
it further, and explain that you'd want to do an otoscopic exam that may 
require sedation or anesthesia, and bacterial cultures.

two things will 
happen. they may listen to you, and bring back dog, and let you work it 
up, or they may go elsewhere and start back at square one. you win some, 
you lose some.

IV catheters without the needles are good to use for ear 
flushing/suctioning. you really need to clean out the ear before you can 
do a complete exam. you want to carefully evaluate skin of vertical and 
horizontal canal. the whole thing. decisions re: longterm management 
evolve not around the culture results, but around the appearance and 
quality of the ear skin of the vertical and horizontal canals. most 
important is the skin of the horizontal canal - if that is irreversibly 
damaged, throwing more stuff down the ear will not help. plus, you are 
really limited wrt surgical options. also you want to evaluate the 
eardrum and look for perforation - if it is perforated, there is likely 
to be middle ear contamination and perhaps otitis media which needs to be 
treated. 

you want to see nice, clean ear canal and intact tympanic 
membrane

examples of products used:
gentocin otic - gentamicin and 
betamethasone
panalog - nystatin, neomycin, thiostrepton, triamcinolone

oti-clens - cleansing solution, ceruminolytic - good to use 
intermittently prophylactically or for maintenance, also to prepare for 
exam
tresaderm - treatment for earmites - thiabendazole, dexamethasone, 
and something else.

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